B51-18 Flecainide Toxicity Leading to Pacemaker Capture Failure and Cardiogenic Shock in a Patient With Sinus Node Dysfunction

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Abstract Introduction Flecainide is a class IC antiarrhythmic commonly utilized in the management of supraventricular arrhythmias, including atrial fibrillation. Due to its narrow therapeutic index and primary renal clearance, flecainide may accumulate with renal impairment, leading to significant electrophysiologic and hemodynamic disturbances. We present a case of flecainide toxicity manifesting with pacemaker capture failure and cardiogenic shock, highlighting the complexity of antiarrhythmic management in the critically ill. Case Presentation 73-year-old woman with paroxysmal atrial fibrillation and sinus node dysfunction managed with a dual-chamber pacemaker was admitted with septic shock and acute kidney injury. Flecainide, previously withheld during the acute illness, was resumed following initial stabilization. Shortly thereafter, the patient developed profound bradycardia with hemodynamic instability. Telemetry and electrocardiography revealed junctional bradycardia with widened QRS complexes and complete atrial and ventricular pacemaker capture failure [Figure 1], despite previously normal device function. Echocardiography demonstrated a newly reduced ejection fraction, raising concern for cardiogenic shock. Flecainide was discontinued due to suspected toxicity. Pacemaker output settings were significantly increased to overcome elevated myocardial capture thresholds, with restoration of appropriate pacemaker capture and hemodynamic recovery, allowing for rapid down-titration and eventual discontinuation of vasopressors. The patient improved with supportive care; renal function recovered, and the patient was discharged on a reduced-dose regimen of flecainide with close-outpatient follow-up. Discussion Flecainide toxicity is a rare, but life-threatening complication, particularly in critically ill patients with acute renal dysfunction, where impaired clearance can lead to accumulation even at maintenance doses. Toxicity may present with bradycardia, QRS prolongation, pacemaker non-capture from elevated myocardial pacing thresholds, and cardiogenic shock due to negative inotropic effects. This toxidrome may be misattributed to device malfunction, and diagnosis is further challenged by limited access to serum flecainide levels, often requiring off-site processing with prolonged turnaround times, as seen in this case. Therefore, clinical context, telemetry, and electrocardiographic findings are essential for timely recognition. Management is supportive, and includes immediate drug cessation, pacemaker output reprogramming to overcome threshold elevations, and temporary transvenous pacing when necessary. Sodium bicarbonate has been proposed as a theoretical adjunct to counter sodium channel blockade through serum alkalinization, though supportive data is limited. Hemodialysis is ineffective due to flecainide’s pharmacokinetic profile. This case underscores the importance of clinical recognition of flecainide toxicity in critically ill patients with renal dysfunction, where early identification and prompt pacemaker interventions are essential in the absence of rapid confirmatory testing. This abstract is funded by: None

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